Acute cholecystitis hospital surgery. Surgery (Acute cholecystitis)

Acute cholecystitis

Acute cholecystitis is inflammation of the gallbladder.

The most acceptable classification of acute cholecystitis is:

I. Uncomplicated cholecystitis:

1. Catarrhal (simple) cholecystitis (calculous or acalculous), primary or exacerbation of chronic recurrent.

2. Destructive (calculous or acalculous), primary or exacerbation of chronic recurrent:

a) phlegmonous, phlegmonous-ulcerative;

b) gangrenous;

II. Complicated cholecystitis:

1. Occlusal (obstructive) cholecystitis (infected dropsy, phlegmon, empyema, gangrene of the gallbladder).

2. Perforated with symptoms of local or diffuse peritonitis.

3. Acute, complicated by damage to the bile ducts:

a) choledocholithiasis, cholangitis;

b) stricture of the common bile duct, papillitis, stenosis of the papilla of Vater.

4. Acute cholecystopancreatitis.

5. Acute cholecystitis, complicated by profuse bile peritonitis.

The main symptom of acute cholecystitis is pain, which usually occurs suddenly in the middle of full health, often after eating, or at night during sleep. The pain is localized in the right hypochondrium, but can also spread to the epigastric region, with irradiation to the right shoulder, scapula, and supraclavicular region. In some cases, before its appearance, patients feel heaviness in the epigastric region, bitterness in the mouth, and nausea for several days, even weeks. Severe pain is associated with the reaction of the gallbladder wall to an increase in its contents as a result of outflow disturbance due to inflammatory edema, kinking of the cystic duct, or blockage of the latter by a stone.

Irradiation of pain to the heart area is often noted, then an attack of cholecystitis can occur as an attack of angina pectoris (Botkin cholecystocoronary syndrome). The pain intensifies with the slightest physical exertion - talking, breathing, coughing.

There is vomiting (sometimes repeated) of a reflex nature, which does not bring relief to the patient.

On palpation, sharp pain and muscle tension are detected in the right upper quadrant of the abdomen, especially sharp pain in the area where the gallbladder is located.

Objective symptoms are not expressed equally in all forms of acute cholecystitis. Increased heart rate up to 100 – 120 beats per minute, symptoms of intoxication (dry, coated tongue) are characteristic of destructive cholecystitis. With complicated cholecystitis, the temperature reaches 38 °C and higher.

When analyzing blood, leukocytosis, neutrophilia, lymphopenia, and increased erythrocyte sedimentation rate are observed.

Specific symptoms of acute cholecystitis include:

1) Grekov-Ortner symptom - percussion pain that appears in the area of ​​the gallbladder when lightly tapping the right costal arch with the edge of the palm;

2) Murphy's symptom - increased pain that occurs when the gallbladder is felt when the patient takes a deep breath. The doctor places the thumb of the left hand below the costal arch, at the location of the gallbladder, and the remaining fingers along the edge of the costal arch. If the patient's deep breath is interrupted before reaching height due to acute pain in the right hypochondrium under the thumb, then Murphy's symptom is positive;

3) Courvoisier’s symptom - an enlargement of the gallbladder is determined by palpation of the elongated part of its bottom, which protrudes quite clearly from under the edge of the liver;

4) Pekarsky’s symptom – pain when pressing on the xiphoid process. It is observed in chronic cholecystitis, its exacerbation and is associated with irritation of the solar plexus during the development of the inflammatory process in the gallbladder;

5) Mussi-Georgievsky symptom (frenicussymptom) - pain on palpation in the supraclavicular region at a point located between the legs of the sternocleidomastoid muscle on the right;

6) Boas symptom - pain on palpation of the paravertebral zone at the level of the IX - XI thoracic vertebrae and 3 cm to the right of the spine. The presence of pain in this place during cholecystitis is associated with zones of Zakharyin-Ged hyperesthesia.

Uncomplicated cholecystitis. Catarrhal (simple) cholecystitis can be calculous or acalculous, primary or as an exacerbation of chronic recurrent cholecystitis. Clinically, in most cases it proceeds calmly. The pain is usually dull and appears gradually in the upper abdomen; intensifying, localized in the right hypochondrium.

On palpation, pain is noted in the area of ​​the gallbladder, and there are also positive Grekov-Ortner and Murphy symptoms. There are no peritoneal symptoms, the number of leukocytes is in the range of 8.0 – 10.0 – 109/l, temperature is 37.6 °C, rarely up to 38 °C, no chills.

Attacks of pain continue for several days, but after conservative treatment they disappear.

Acute destructive cholecystitis can be calculous or acalculous, primary or an exacerbation of chronic recurrent cholecystitis.

Destruction can be phlegmonous, phlegmonous-ulcerative or gangrenous in nature.

With phlegmonous cholecystitis, the pain is constant and intense. Dry tongue, repeated vomiting. There may be a slight yellowness of the sclera and soft palate, which is due to infiltration of the hepatoduodenal ligament and inflammatory swelling of the mucous membrane of the bile ducts. Urine is dark brown. Patients lie on their backs or on their right side, afraid to change their position in the back, since in this case severe pain occurs. On palpation of the abdomen, a sharp tension in the muscles of the anterior abdominal wall in the area of ​​the right hypochondrium is observed, and positive Grekov-Ortner, Murphy, Shchetkin-Blumberg symptoms also occur there. The temperature reaches 38 °C and higher, leukocytosis is 12.0 – 16.0 – 109 / l with a shift in the leukocyte formula to the left. When the inflammatory process spreads to the entire gallbladder and pus accumulates in it, gallbladder empyema is formed.

Sometimes phlegmonous cholecystitis can develop into hydrocele of the gallbladder.

Gangrenous cholecystitis in most cases is a transitional form of phlegmonous, but can also occur as an independent disease in the form of primary gangrenous cholecystitis of vascular origin.

Clinic at first it corresponds to phlegmonous inflammation, then so-called imaginary well-being may occur: pain decreases, symptoms of peritoneal irritation are less pronounced, and temperature decreases. However, at the same time, the phenomena of general intoxication increase: rapid pulse, dry tongue, repeated vomiting, sharpened facial features.

Primary gangrenous cholecystitis from the very beginning proceeds rapidly with symptoms of intoxication and peritonitis.

Complicated cholecystitis. Occlusive (obstructive) cholecystitis develops when the cystic duct is blocked by a calculus and initially manifests itself with a typical picture of biliary colic, which is the most characteristic sign of cholelithiasis. Sharp pain occurs suddenly in the right hypochondrium with irradiation to the right shoulder, scapula, heart area and behind the sternum. Patients behave restlessly; at the height of the attack, vomiting appears, sometimes multiple times. The abdomen may be soft, while a sharply painful, enlarged and tense gallbladder can be palpated.

An attack of biliary colic can last several hours or 1–2 days and, when the stone passes back into the gallbladder, end suddenly. With prolonged blockage of the cystic duct and infection, destructive cholecystitis develops.

Perforated cholecystitis occurs with symptoms of local or diffuse peritonitis. The moment of perforation of the gallbladder may go unnoticed by the patient. If neighboring organs are soldered to the gallbladder - the greater omentum, hepatoduodenal ligament, transverse colon and its mesentery, i.e. the process is limited, then complications such as subhepatic abscess and local limited peritonitis develop.

Acute cholecystitis, complicated by damage to the bile ducts, can occur with clinical manifestations of choledocholithiasis, cholangitis, stricture of the common bile duct, papillitis, stenosis of the papilla of Vater. The main symptom of this form is obstructive jaundice, the most common cause of which is stones of the common bile duct obstructing its lumen.

When the common bile duct is blocked by a stone, the disease begins with acute pain, characteristic of acute calculous cholecystitis, with typical irradiation. Then, after a few hours or the next day, obstructive jaundice appears, becoming persistent, accompanied by severe itching, dark urine and discolored (acholic) putty-like feces.

As a result of infection and its spread to the bile ducts, symptoms of acute cholangitis develop. Acute purulent cholangitis is characterized by symptoms of severe intoxication - general weakness, lack of appetite, icteric discoloration of the skin and mucous membranes. Constant dull pain in the right hypochondrium with irradiation to the right half of the back, heaviness in the area of ​​the right hypochondrium, when tapping along the right costal arch - sharp pain. Body temperature rises in a remitting manner, with profuse sweating and chills. The tongue is dry and coated. On palpation, the liver is enlarged, painful, and has a soft consistency. Leukocytosis with a shift of the leukocyte formula to the left is noted. In a biochemical blood test, an increase in the content of direct bilirubin and a decrease in the content of prothrombin in the blood plasma is observed. The disease can be complicated by life-threatening cholemic bleeding and liver failure.

Differential diagnosis. Acute cholecystitis must be differentiated from a perforated gastric and duodenal ulcer, acute pancreatitis, acute appendicitis, acute coronary insufficiency, myocardial infarction, acute intestinal obstruction, pneumonia, pleurisy, thrombosis of mesenteric vessels, kidney stones localized in the right kidney or right ureter, and also with liver diseases (hepatitis, cirrhosis) and biliary dyskinesia.

Biliary dyskinesia must be differentiated from acute cholecystitis, which is of practical importance for the surgeon in the treatment of this disease. Biliary dyskinesia is a violation of their physiological functions, leading to stagnation of bile in them, and subsequently to disease. Dyskinesia in the biliary tract mainly consists of disorders of the gallbladder and the closing apparatus of the lower end of the common bile duct.

TO dyskinesia include:

1) atonic and hypotonic gallbladders;

2) hypertensive gall bladders;

3) hypertension and spasm of the sphincter of Oddi;

4) atony and insufficiency of the sphincter of Oddi.

The use of cholangiography before surgery makes it possible to recognize the main types of these disorders in patients.

Duodenal intubation makes it possible to establish a diagnosis of atonic gallbladder if there is an abnormally abundant flow of intensely colored bile, occurring immediately or only after the second or third administration of magnesium sulfate.

When cholecystography is performed with the patient lying on his stomach, the cholecystogram shows a picture of a flabby elongated bladder, expanded and giving a more intense shadow at the bottom, where all the bile collects.

When a diagnosis of “acute cholecystitis” is made, the patient must be urgently hospitalized in a surgical hospital. All operations for acute cholecystitis are divided into emergency, urgent and delayed. Emergency operations are carried out for health reasons in connection with a clear diagnosis of perforation, gangrene or phlegmon of the gallbladder, emergency operations - if vigorous conservative treatment is unsuccessful during the first 24 - 48 hours from the onset of the disease.

Operations are performed within 5 to 14 days and later when an attack of acute cholecystitis subsides and an improvement in the patient’s condition is observed, i.e. in the phase of decreasing the severity of the inflammatory process.

The main operation in the surgical treatment of acute cholecystitis is cholecystectomy, which, according to indications, is supplemented by external or internal drainage of the biliary tract. There is no reason to expand the indications for cholecystostomy.

Indications for choledochotomy are obstructive jaundice, cholangitis, obstruction of patency in the distal parts of the common bile duct, stones in the ducts.

A blind suture of the common bile duct is possible with full confidence in the patency of the duct and, as a rule, with single large stones. External drainage of the common bile and hepatic ducts is indicated in cases of cholangitis with patency of the distal duct.

Indications for the application of biliodigestive anastomosis are lack of confidence in the patency of the papilla of Vater, indurative pancreatitis, and the presence of multiple small stones in the ducts in patients. Biliodigestive anastomosis can be performed in the absence of pronounced inflammatory changes in the anastomosed organs by a highly qualified surgeon. In other conditions, one should limit oneself to external drainage of the biliary tract.

Management of patients in the postoperative period must be strictly individualized. You are allowed to get up after 24 hours; you are discharged and the stitches are removed after about 10 to 12 days.

RUSSIAN STATE

MEDICAL UNIVERSITY

Department of Hospital Surgery

Head Department Professor Nesterenko Yu.P.

Teacher Andreytseva O.I.

Essay

Subject: "Acute cholecystitis."

Completed by a fifth year student

Faculty of Medicine

511 a gr. Krat V.B.

Moscow

Acute cholecystitis is an inflammatory process in the extrahepatic tract with a predominant lesion of the gallbladder, in which there is a disruption of the nervous regulation of the production of the liver and biliary tract, as well as changes in the biliary tract themselves due to inflammation, bile stagnation and cholesterolemia.

Depending on the pathological changes, catarrhal, phlegmonous, gangrenous and perforated cholecystitis are distinguished.

The most common complications of acute cholecystitis are encysted and diffuse purulent peritonitis, cholangitis, pancreatitis, and liver abscesses. In acute calculous cholecystitis, partial or complete blockage of the common bile duct may occur with the development of obstructive jaundice.

There are acute cholecystitis that developed for the first time (primary acute cholecystitis) or due to chronic cholecystitis (acute recurrent cholecystitis). For practical use, the following classification of acute cholecystitis can be recommended:

I Acute primary cholecystitis (calculous, acalculous): a) simple; b) phlegmonous; c) gangrenous; d) perforative; e) complicated cholecystitis (peritonitis, cholangitis, bile duct obstruction, liver abscess, etc.).

II Acute secondary cholecystitis (calculous and acalculous): a) simple; b) phlegmonous; c) gangrenous; d) perforative; e) complicated (peritonitis, cholangitis, pancreatitis, bile duct obstruction, liver abscess, etc.).

Etiology and pathogenesis of acute cholecystitis:

The inflammatory process in the wall of the gallbladder can be caused not only by a microorganism, but also by a certain composition of food, allergic and autoimmune processes. In this case, the integumentary epithelium is reconstructed into goblet and mucous membranes, which produce a large amount of mucus, the cylindrical epithelium is flattened, microvilli are lost, and absorption processes are disrupted. In the niches of the mucosa, water and electrolytes are absorbed, and colloidal solutions of mucus are converted into a gel. When the bladder contracts, lumps of gel slip out of their niches and stick together, forming the rudiments of gallstones. The stones then grow and saturate the center with pigment.

The main reasons for the development of the inflammatory process in the wall of the gallbladder are the presence of microflora in the cavity of the bladder and a violation of the outflow of bile. The main importance is given to infection. Pathogenic microorganisms can enter the bladder in three ways: hematogenous, lymphogenous, enterogenous. The following organisms are most often found in the gallbladder: E.coli, Staphilococcus, Streptococcus.

The second reason for the development of the inflammatory process in the gallbladder is a violation of the outflow of bile and its stagnation. In this case, mechanical factors play a role - stones in the gallbladder or its ducts, kinks in the elongated and tortuous cystic duct, and its narrowing. According to statistics, up to 85-90% of cases of acute cholecystitis occur against the background of cholelithiasis. If sclerosis or atrophy develops in the bladder wall, the contractile and drainage functions of the gallbladder suffer, which leads to a more severe course of cholecystitis with profound morphological disorders.

Vascular changes in the wall of the bladder play an absolute role in the development of cholecystitis. The rate of development of inflammation, as well as morphological disturbances in the wall, depend on the degree of circulatory disturbance.

Clinic of acute cholecystitis:

The clinical picture of acute cholecystitis depends on the pathological changes in the gallbladder, the duration and course of the disease, the presence of complications and the reactivity of the body. The disease usually begins with an attack of pain in the gallbladder area. The pain radiates to the right shoulder, right supraclavicular space and right scapula, to the right subclavian region. A painful attack is accompanied by nausea and vomiting mixed with bile. As a rule, vomiting does not bring relief.

The temperature rises to 38-39°C, sometimes with chills. In elderly and senile people, severe destructive cholecystitis can occur with a slight increase in temperature and moderate leukocytosis. With simple cholecystitis, the pulse quickens according to the temperature; with destructive and, especially, perforative cholecystitis with the development of peritonitis, tachycardia is noted up to 100-120 beats per minute.

During examination, patients have icteric sclera; severe jaundice occurs when the patency of the common bile duct is impaired due to obstruction by a stone or inflammatory changes.

The abdomen is painful on palpation in the area of ​​the right hypochondrium. In the same area, muscle tension and symptoms of peritoneal irritation are determined, especially pronounced in destructive cholecystitis and the development of peritonitis.

There is pain when tapping along the right costal arch (Grekov-Ortner symptom), pain when pressing or tapping in the area of ​​the gallbladder (Zakharyin’s symptom) and with deep palpation when the patient inhales (Obraztsov’s symptom). The patient cannot take a deep breath with deep palpation in the right hypochondrium. Pain on palpation in the right supraclavicular region is characteristic (Georgievsky's symptom).

In the initial stages of the disease, careful palpation can reveal an enlarged, tense and painful gallbladder. The latter is especially well contoured during the development of acute cholecystitis due to hydrocele of the gallbladder. In case of gangrenous, perforated cholecystitis, due to severe tension in the muscles of the anterior abdominal wall, as well as in case of exacerbation of sclerosing cholecystitis, it is not possible to palpate the gallbladder. In severe destructive cholecystitis, sharp pain is observed during superficial palpation in the area of ​​the right hypochondrium, light tapping and pressing on the right costal arch.

A blood test reveals neutrophilic leukocytosis (10 – 20 x 10 9 /l), with jaundice hyperbilirubinemia.

The course of acute simple primary acalculous cholecystitis in 30-50% of cases ends with recovery within 5-10 days after the onset of the disease. Although acute cholecystitis can be very severe with the rapid development of gangrene and perforation of the bladder, especially in elderly and senile people. With exacerbation of chronic calculous cholecystitis, stones can contribute to faster destruction of the bladder wall due to stagnation and the formation of bedsores.

However, much more often, inflammatory changes increase gradually; within 2-3 days, the nature of the clinical course is determined with the progression or subsidence of inflammatory changes. Consequently, there is usually enough time to assess the course of the inflammatory process, the patient’s condition and a reasonable method of treatment.

Differential diagnosis:

Acute cholecystitis is differentiated from the following diseases:

1) Acute appendicitis. In acute appendicitis, the pain is not so intense, and, most importantly, does not radiate to the right shoulder, right scapula, etc. Also, acute appendicitis is characterized by migration of pain from the epigastrium to the right iliac region or throughout the abdomen; with cholecystitis, the pain is precisely localized in the right hypochondrium ; vomiting with appendicitis is one-time. Typically, palpation reveals a thickened consistency of the gallbladder and local tension in the muscles of the abdominal wall. Ortner's and Murphy's symptoms are often positive.

2) Acute pancreatitis. This disease is characterized by girdling pain and sharp pain in the epigastrium. A positive Mayo-Robson sign is noted. The patient's condition is characteristically grave; he assumes a forced position. The level of diastase in urine and blood serum is of decisive importance in diagnosis; figures above 512 units are conclusive. (in urine).

With stones in the pancreatic duct, the pain is usually localized in the left hypochondrium.

3) Acute intestinal obstruction. In acute intestinal obstruction, the pain is cramping and non-localized. There is no increase in temperature. Enhanced peristalsis, sound phenomena (“splashing noise”), and radiological signs of obstruction (Kloiber cups, arcades, symptom of pinnateness) are absent in acute cholecystitis.

4) Acute obstruction of the mesenteric arteries. With this pathology, severe pain of a constant nature occurs, but usually with distinct intensification, and is less diffuse in nature than with cholecystitis (more diffuse). A history of pathology of the cardiovascular system is required. The abdomen is easily accessible for palpation, without pronounced symptoms of peritoneal irritation. Fluoroscopy and angiography are decisive.

5) Perforated ulcer of the stomach and duodenum. Men are more likely to suffer from this, while cholecystitis most often affects women. Cholecystitis is characterized by intolerance to fatty foods, frequent nausea and malaise, which does not happen with a perforated ulcer of the stomach and duodenum; pain is localized in the right hypochondrium and radiates to the right scapula, etc., with an ulcer the pain radiates mainly to the back. Erythrocyte sedimentation is accelerated (with an ulcer - vice versa). The picture is clarified by the presence of a history of ulcers and tarry stools. X-ray reveals free gas in the abdominal cavity.

6) Renal colic. Pay attention to the urological history. The kidney area is carefully examined, Pasternatsky's symptom is positive, a urine test, excretory urography, and chromocystography are performed to clarify the diagnosis, since renal colic often provokes biliary colic.

Inflammation of the gallbladder.
The 2 hepatic ducts merge at the porta hepatis into the common hepatic duct. It connects to the bladder, which drains bile from the gallbladder. Merging they form the COLEDOCH (common bile duct). It passes in the hepatoduodenal ligament to the right of the a.hetatica and in front of the v.porte, in the middle third of the 12th. The common bile duct pierces its posteromedial wall and opens into the intestinal lumen at the apex of the papilla of Vater, together with the excretory duct of the pancreas.

In pathogenesis, of particular importance is the disruption of the blood supply to the wall of the gallbladder (in patients with AS, diabetes against the background of AS injuries, thrombosis of the branches or trunk of the cystic artery is possible, leading to foci of neurosis and perforation).

Classification.

According to the development mechanism:

  1. calculous
  2. stoneless

According to morphological changes:

  1. Catarrhal
  2. Destructive: phlegmatic and gangrenous.

According to the presence of complications:

  1. occlusive (obstructive): infected dropsy, phlegmon, empyema, gangrene.
  2. perforated with symptoms of peritonitis.
  3. acute, complicated by damage to the bile ducts: choledocholethiasis, cholangitis.
  4. acute cholecystopancreatitis
  5. acute cholecystitis complicated by bile peritonitis.

Clinic.

Catarrhal cholecystitis.

The patient's condition suffers little. Body temperature is subfibrile, moderate pain in the right hypochondrium, radiating to the right scapula and shoulder. Symptoms of intoxication are not pronounced, there is a slight tachycardia (no more than 90 beats per minute). Dyspeptic disorders manifest themselves in the form of nausea and flatulence. Vomiting is not typical.

Palpation of the abdomen reveals moderate pain in the right hypochondrium without symptoms of peritoneal irritation.

In the blood there is a slight increase in the number of leukocytes to 9 - 11 / l. no formula changes.

Phlegmonous cholecystitis.

The general condition of the patient suffers, weakness, fever, dry mouth, oliguria, tachycardia up to 100 beats appear. per minute The pain syndrome is pronounced, with characteristic irradiation. Dyspeptic syndrome is characterized by nausea, repeated vomiting, and bloating.

Upon examination, the tongue is dry and coated with a yellow-gray coating. On palpation - pain in the right hypochondrium, epigastric region. Here, tension in the muscles of the anterior abdominal wall is observed, and symptoms of peritoneal irritation are noted. In more than half of patients, a subhepatic infiltrate or an enlarged gallbladder is palpable. The latter indicates the development of empyema of the gallbladder. Since with phlegmonous cholecystitis the surrounding tissues are involved in the inflammatory process, a perivesical infiltrate is formed. If the latter does not occur, peritonitis of varying degrees of prevalence may develop.

Gangrenous cholecystitis.

The pain is pronounced, does not have a typical localization, and is often distributed throughout the abdomen. Symptoms of general intoxication predominate - patients are adynamic or agitated. Tachycardia more than 110 beats. per minute Repeated vomiting and sequestration of fluid into the abdominal cavity lead to rapid dehydration. The tongue is dry, the abdomen is moderately swollen due to intestinal paresis, painful on palpation in all parts with symptoms of peritoneal irritation.

The clinical picture of the disease progresses rapidly, which is associated with the development of peritonitis.

The diagnosis is made based on:

1. Patient’s complaints, medical history.

1. Clinical data:

Grekov–Ortner sign– percussion pain in the area of ​​the gallbladder with light tapping on the right costal arch.

- Murphy's symptom - increased pain with deep inspiration.

Courvoisier's sign - The bottom of the enlarged gallbladder is determined.

— Kera symptom – pain when inhaling during palpation in the right hypochondrium.

Obraztsov's symptom– when you insert your hand into the right hypochondrium while inhaling, the pain intensifies.

Mussi–Georgievsky sign– pain in the supraclavicular area between the legs of the sternocleidoid – mastoid muscle on the right.

— Aschoff's symptom is a congestive gallbladder, manifested by biliary colic, nausea, and vomiting. It is observed when there is an obstruction to the outflow of bile.

Courvoisier's triad– the bottom of the enlarged gallbladder is palpated, the presence of obstructive jaundice and high body temperature.

1. Laboratory diagnostics:

- general blood analysis

- general urine analysis

- bilirubin

- transaminases

1. Instrumental diagnostic methods:

Duodenal sounding - portion B - bladder bile with inflammation will be cloudy with mucus and flakes.

— Ultrasound

— Overview R – graphics

- Cholecystography - slow emptying of the gallbladder.

— Retragrade cholangiography (using an endoscope, we find the large duodenal papilla and cannulate it, injecting a contrast agent.)

Treatment.

Conservative treatment:

— antibacterial therapy (antibacterial treatment options using one of them)

— For severe pain, use baralgin injections (5 ml).

— infusion therapy — Hemodesis.

Surgical treatment:

Classification of surgical interventions:

1. Emergency operations Surgical interventions performed in the first hours of the patient’s hospital stay after short-term preoperative preparation and examination should be considered. Preparation for the operation should not exceed 4–6 hours and is carried out jointly with the anesthesiologist and therapist. The indication for emergency surgery is the presence of widespread peritonitis in the patient.

2. Urgent operations Surgical interventions performed within the first 24 to 48 hours after admission to the hospital should be considered. Indications for urgent surgery are destructive forms of cholecystitis identified during initial ultrasound or developing during dynamic observation. Optimal conditions for the technical implementation of these operations are no more than 5 days, because at a later date, infiltrative changes develop in the area of ​​the gallbladder and hepatoduodenal ligament, which leads to difficulty in surgical intervention.

3. Deferred operations in acute cholecystitis, interventions should be considered within a period exceeding 3 days after the positive effect of drug treatment and a comprehensive clinical examination.

Types of surgical intervention:

— cholecystostomy (surgical operation: application of an external fistula of the gallbladder; used in cases of acute cholecystitis when the patient’s condition does not allow more complex surgical intervention)

— cholecystectomy

— laparoscopic cholecystectomy

Surgical access. For access to the gallbladder and extrahepatic bile ducts, the most convenient are incisions in the right hypochondrium (Kocher, Fedorova). In some cases, upper-middle laparotomy is acceptable.

When performing cholecystectomy by laparotomy, two methods are used to remove the gallbladder - from the neck and from the bottom. Preference should be given to cholecystectomy from the cervix with separate ligation of the cystic artery and cystic duct. Ligation of the cystic artery before mobilization of the gallbladder significantly reduces blood loss. Ligation of the cystic duct avoids the migration of small stones from the bladder into the biliary tract. After removal of the gallbladder and hemostasis, the gallbladder bed is carefully inspected and sutured with catgut with good adaptation of the edges of the liver wound.

In case of purulent destructive processes of the gallbladder, its bed is not sutured. After hemostasis, drainage and, if necessary, a tampon are supplied to the bed.

Cholecystectomy from the fundus, as a rule, is a forced intervention option in the presence of infiltration in the area of ​​the hepatoduodenal ligament and the neck of the gallbladder.

Long-term results of cholecystectomy for acute cholecystitis are quite favorable. After 1.5 – 2 months, in 90–95% of observations, patients return to their previous work and dietary regime. These periods are significantly reduced when cholecystectomy is performed laparoscopically.

State budgetary educational institution of higher professional education

"Tyumen State Medical AcademyMinistry of Health of the Russian Federation"

DEPARTMENT OF FACULTY SURGERY WITH A COURSE OF UROLOGY

ACUTE CHOLECYSTITIS AND ITS COMPLICATIONS

Module 2. Diseases of the bile ducts and pancreas

Methodological guide for preparing for the exam in faculty surgery and the Final State Certification of students of the Faculty of Medicine and Pediatrics

Compiled by: DMN, prof. N. A. Borodin

Tyumen - 2013

ACUTE CHOLECYSTITIS

Questions that a student should know about the topic:

Acute cholecystitis. Etiology, classification, diagnosis, clinical picture. Choice of treatment method. Methods of surgical and conservative treatment.

Acute obstructive cholecystitis, definition of the concept. Clinic, diagnosis, treatment.

Hepatic colic and acute cholecystitis, differential diagnosis, clinical picture, methods of laboratory and instrumental studies. Treatment.

Acute cholecystopancreatitis. Causes of occurrence, clinical picture, methods of laboratory and instrumental studies. Treatment.

Choledocholithiasis and its complications. Purulent cholangitis. Clinical picture, diagnosis and treatment.

Surgical complications of opisthorchiasis of the liver and gall bladder. Pathogenesis, clinical picture, treatment.

Acute cholecystitis This is an inflammation of the gallbladder from catarrhal to phlegmonous and gangrenous-perforated.

In emergency surgery, the concept of “chronic cholecystitis” or “exacerbation of chronic cholecystitis” is usually not used, even if this was not the patient’s first attack. This is due to the fact that in surgery any acute attack of cholecystitis is considered as a phase of a destructive process that can result in purulent peritonitis. The term “chronic calculous cholecystitis” is used almost only in one case, when the patient is admitted for planned surgical treatment in the “cold” period of the disease.

Acute cholecystitis is most often a complication of cholelithiasis (acute calculous cholecystitis). Often the trigger for the development of cholecystitis is a violation of the outflow of bile from the bladder under the influence of stones, then an infection occurs. A stone can completely block the neck of the gallbladder and completely “turn off” the gallbladder; this cholecystitis is called “obstructive”.

Much less often, acute cholecystitis can develop without gallstones - in this case it is called acute acalculous cholecystitis. Most often, such cholecystitis develops against the background of impaired blood supply to the gallbladder (atherosclerosis or thrombosis a.cistici) in elderly people; the cause may also be reflux of pancreatic juice into the gallbladder - enzymatic cholecystitis.

Classification of acute cholecystitis.

Uncomplicated cholecystitis

1. Acute catarrhal cholecystitis

2. Acute phlegmonous cholecystitis

3. Acute gangrenous cholecystitis

Complicated cholecystitis

1. Peritonitis with perforation of the gallbladder.

2. Peritonitis without gallbladder perforation (sweaty biliary peritonitis).

3. Acute obstructive cholecystitis (cholecystitis against the background of obstruction of the neck of the gallbladder in the area of ​​its neck, i.e. against the background of a “switched off” gallbladder. The usual cause is a stone wedged into the area of ​​the neck of the bladder. With catarrhal inflammation this takes on the character hydrocele of the gallbladder, with a purulent process occurs gallbladder empyema, i.e. accumulation of pus in the disabled gallbladder.

4. Acute cholecysto-pancreatitis

5. Acute cholecystitis with obstructive jaundice (choledocholithiasis, strictures of the major duodenal papilla).

6. Purulent cholangitis (spread of purulent process from the gallbladder to the extrahepatic and intrahepatic bile ducts)

7. Acute cholecystitis against the background of internal fistulas (fistulas between the gallbladder and intestines).

Clinical picture.

The disease begins acutely as an attack of hepatic colic (hepatic colic is described in the manual on cholelithiasis), when an infection occurs, a clinical picture of the inflammatory process and intoxication develops, and the progressive disease leads to local and diffuse peritonitis.

The pain occurs suddenly, patients become restless and do not find rest. The pain itself is constant and increases as the disease progresses. Localization of pain is the right hypochondrium and epigastric region, the most severe pain is in the projection of the gallbladder (Ker's point). Irradiation of pain is typical: in the lower back, under the angle of the right shoulder blade, in the supraclavicular region on the right, in the right shoulder. Often a painful attack is accompanied by nausea and repeated vomiting, which does not bring relief. A subfibrile temperature appears, sometimes accompanied by chills. The last sign may indicate the addition of cholestasis and the spread of the inflammatory process to the bile ducts.

On examination: the tongue is coated and dry, the abdomen is painful in the right hypochondrium. The appearance of tension in the muscles of the anterior abdominal wall in the right hypochondrium (village Kerte) and symptoms of peritoneal irritation (Shchetkina-Blumberga village) speaks of the destructive nature of inflammation.

In some cases (with obstructive cholecystitis), you can feel an enlarged, tense and painful gallbladder.

Symptoms of acute cholecystitis

Ortner-Grekov symptom– pain when tapping the edge of the palm on the right costal arch.

Zakharyin's symptom– pain when tapping the edge of the palm in the right hypochondrium.

Murphy's sign– when pressing on the area of ​​the gallbladder with the fingers, the patient is asked to take a deep breath. In this case, the diaphragm moves down and the stomach rises, the bottom of the gallbladder collides with the examiner’s fingers, severe pain occurs and breathing is interrupted.

In modern conditions, Murphy's symptom can be checked during an ultrasound examination of the bladder; an ultrasound sensor is used instead of a hand. You need to press the sensor on the anterior abdominal wall and force the patient to take a breath; the device screen shows how the bubble approaches the sensor. When the device approaches the bladder, severe pain occurs and the patient interrupts his breath.

Mussi-Georgievsky's sign(phrenicus symptom) - the occurrence of painful sensations when pressing in the area of ​​the sternocleidomastoid muscle, between its legs.

Ker's symptom- pain when pressing with a finger into the angle formed by the edge of the right rectus abdominis muscle and the costal arch.

Pain on palpation of the right hypochondrium is called Obraztsov's symptom, but since it resembles other symptoms, sometimes this sign is called the Kera-Obraztsev-Murphy symptom.

Pain when pressing on the xiphoid process is called the xiphoid process phenomenon or Likhovitsky's symptom.

Laboratory research. Acute cholecystitis is characterized by an inflammatory reaction of the blood, primarily leukocytosis. With the development of peritonitis, leukocytosis becomes pronounced - 15-20 10 9 /l, the band shift of the formula increases to 10-15%. Severe and advanced forms of peritonitis, as well as purulent cholangitis, are accompanied by a shift of the formula “to the left” with the appearance of young forms and myelocytes.

Other blood counts change when complications occur (see below).

Instrumental research methods.

There are several methods for instrumental diagnosis of bile duct diseases, mainly ultrasound and radiological methods (ERCP, intraoperative cholangiography and postoperative fistulocholangiography). Computed tomography is rarely used to examine the bile ducts. This is written in detail in the Guidelines on cholelithiasis and methods for studying the bile ducts. It should be noted that for the diagnosis of cholelithiasis and diseases associated with impaired bile outflow, both ultrasound and x-rays are usually used. methods, but to diagnose inflammatory changes in the gallbladder and surrounding tissues - only ultrasound.

At acute cholecystitis, the ultrasound picture is as follows. Most often, acute cholecystitis occurs against the background of cholelithiasis, therefore, in most cases, an indirect sign of cholecystitis is the presence of stones in the gall bladder, or bile sludge or pus, which are determined in the form of suspended small particles without an acoustic shadow.

Often acute cholecystitis occurs against the background of obstruction of the neck of the gallbladder; this cholecystitis is called Obstructive; on ultrasound it is visible as an increase in the longitudinal (more than 90-100 mm) and transverse direction (up to 30 mm or more). Finally straight Ultrasound signs of destructive cholecystitis is: thickening of the bladder wall (normally 3 mm) to 5 mm or more, stratification (doubling) of the wall, the presence of a strip of liquid (effusion) next to the gallbladder under the liver, signs of inflammatory infiltration of surrounding tissues.

14319 0

Acute cholecystitis - acute inflammation of the gallbladder of a bacterial nature.

ICD-10 CODE
K81.0. Acute cholecystitis.

Epidemiology

Acute cholecystitis is one of the most common diseases of the abdominal organs and ranks second after acute appendicitis. The high incidence is associated with an increase in the incidence of cholelithiasis (GSD) and an increase in people's life expectancy. The disease is more common in people over 50 years of age; elderly and senile patients account for more than 50%; The ratio of men to women among patients is approximately 1:5.

Classification

The classification of acute cholecystitis is of practical importance for making the right tactical decision that is adequate to a specific clinical situation. The classification is based on the clinical and morphological principle of the dependence of the clinical manifestations of the disease on pathomorphological changes in the gallbladder, extrahepatic bile ducts and the abdominal cavity. In this classification, there are two groups of acute cholecystitis - uncomplicated And complicated.

Clinical and morphological classification of acute cholecystitis
Form of cholecystitis:

  • catarrhal;
  • phlegmonous;
  • gangrenous.
Complications:
  • peri-vesical infiltrate;
  • perivesical abscess;
  • perforation of the gallbladder;
  • peritonitis;
  • obstructive jaundice;
  • cholangitis;
  • external or internal bile fistula.
Uncomplicated acute cholecystitis includes all pathomorphological forms of inflammation of the gallbladder that are routinely encountered in clinical practice. This is catarrhal, phlegmonous and gangrenous inflammation. Each of these forms should be considered as a natural development of the inflammatory process: a gradual transition from the catarrhal process of inflammation to gangrene.

With this mechanism of development of the pathological process, foci of necrosis of various sizes arise against the background of phlegmonous changes in the gallbladder as a result of vascular disorders.

An exception to this pattern is primary gangrenous cholecystitis, since its origin is based on impaired blood circulation in the wall of the gallbladder (atherothrombosis). In primary gangrenous cholecystitis, the entire gallbladder undergoes necrosis at once, its walls are thinned, parchment-type and black in color.

Enzymatic cholecystitis, which develops as a result of reflux of pancreatic secretions into the gallbladder, is relatively rare, which can occur in the presence of a common ampulla of the bile duct and the pancreatic duct. With enzymatic cholecystitis, the mucous membrane of the gallbladder is primarily damaged, and infection is secondary.

Etiology and pathogenesis

The occurrence of acute cholecystitis is associated with two main factors: infection of the bile or gallbladder wall and bile stasis (biliary hypertension). Only when they are combined do conditions for the development of the inflammatory process are created. Infection enters the gallbladder in three ways - hematogenous, lymphogenous and enterogenous. In most cases, infection occurs hematogenously: from the general circulation through the common hepatic artery system or from the gastrointestinal tract through the portal vein. With a decrease in the phagocytic activity of the reticuloendothelial system of the liver, microorganisms enter the bile capillaries through the cell membranes and, with the flow of bile, into the gallbladder. Usually they are located in the wall of the gallbladder, in the ducts of Luschka, so often microbial flora may not be detected in the gallbladder bile.

The second decisive factor in the development of acute cholecystitis is bile stagnation, which most often occurs due to stone obstruction of the neck of the gallbladder or cystic duct. Stones, being in the cavity of the gallbladder, do not create an obstacle to the outflow of bile. However, if the diet is violated, the contractility of the gallbladder increases and obstruction of the neck or cystic duct may occur. Less commonly, biliary stasis is caused by blockage of the cystic duct with lumps of mucus, putty-like detritus, and stagnation can also occur when the gallbladder is narrowed and kinked. Intravesical biliary hypertension following the blockade causes the development of an inflammatory process in the gallbladder. In 70% of patients, stone obstruction leads to stagnation of bile and biliary hypertension, which allows us to consider cholelithiasis as the main factor predisposing to the development of acute “obstructive” cholecystitis.

Lysolecithin is of great importance in the pathogenesis of the inflammatory process, high concentrations of which are formed in the bile during blockade of the gallbladder, accompanied by damage to its mucosa and the release of phospholipase A 2. This tissue enzyme converts bile lecithin into lysolecithin; together with bile salts, it damages the mucous membrane of the gallbladder, causes disruption of the permeability of cell membranes and changes in the colloidal state of bile. As a result of these processes, aseptic inflammation of the gallbladder wall occurs.

In conditions of biliary hypertension, when the gallbladder is stretched, mechanical compression of the vessels occurs, microcirculation disturbances occur, blood flow slows down and stasis in the capillaries, venules, and arterioles. The degree of vascular disorders in the gallbladder wall is directly dependent on the severity of biliary hypertension. If elevated pressure persists, then due to ischemia of the gallbladder wall and changes in the qualitative composition of bile, the endogenous infection becomes virulent.

Exudation into the lumen of the gallbladder that occurs during inflammation contributes to the progression of intravesical hypertension and even greater damage to the mucosa. In this case, we can talk about the formation of a pathophysiological vicious circle, in which the primary link in the development of the inflammatory process is considered to be acute biliary hypertension, and the secondary is infection.

The timing and severity of the inflammatory process in the gallbladder largely depend on vascular disorders in its wall. They lead to the appearance of foci of necrosis, most often occurring in the fundus or neck, followed by perforation of the bladder wall. In elderly patients, impaired circulation in the gallbladder against the background of atherosclerosis and hypertension especially often causes the development of destructive forms of acute cholecystitis. With atherothrombosis or cystic artery embolism, such patients may develop primary gangrene of the gallbladder.

Clinical picture

Clinical symptoms of acute cholecystitis depend on pathomorphological changes in the gallbladder, the presence and prevalence of peritonitis, as well as the nature of the concomitant pathology of the bile ducts. The diversity of the clinical picture of the disease can create diagnostic difficulties and cause errors.

Acute cholecystitis occurs suddenly and manifests with severe constant abdominal pain, the intensity of the pain increases as the disease progresses. The development of acute inflammatory phenomena in the gallbladder is often preceded by attack of biliary colic. The localization of pain in the right hypochondrium and epigastric region is typical. It is often noted irradiation to the right shoulder, supraclavicular region, interscapular space or in the heart region. The latter localization can be regarded as an attack of angina (cholecystocoronary symptom of S.P. Botkin), and also provoke its occurrence.

Constant symptoms of acute cholecystitis are nausea and repeated vomiting, which does not bring relief to the patient. An increase in body temperature is noted from the first days of the disease, its nature depends on the pathomorphological changes in the gallbladder. Destructive forms of acute cholecystitis are characterized by chills.

The general condition of the patient upon admission to the hospital depends on the form of the disease. The skin is usually of normal color. Moderate icterus of the sclera may be caused by the transition of the inflammatory process from the gallbladder to the liver and the development of local toxic hepatitis. The appearance of icterus in the sclera and skin is a sign of the mechanical nature of extrahepatic cholestasis (choledocholithiasis, stenosis of the major duodenal papilla). This must be taken into account when determining treatment tactics.

The pulse rate ranges from 80 to 120 per minute and higher. A rapid pulse is a symptom indicating developing intoxication and inflammatory changes in the gallbladder and abdominal cavity.

In acute cholecystitis, you can identify:

  • Ortner's symptom - sharp pain in the projection of the gallbladder when lightly tapping the edge of the palm along the right costal arch;
  • Murphy's symptom - involuntary holding of breath while inhaling when pressing on the area of ​​the right hypochondrium;
  • Kehr's symptom - increased pain on inspiration with deep palpation of the right hypochondrium;
  • Georgievsky-Mussi symptom (phrenicus symptom) - pain on the right when pressing between the legs of the sternocleidomastoid muscle;
  • Shchetkin-Blumberg symptom - becomes positive if the peritoneum is involved in the inflammatory process.
The frequency of detection of the above symptoms depends on the severity of the inflammatory process in the gallbladder (a form of acute cholecystitis) and the involvement of the peritoneum. As the inflammatory process in the gallbladder progresses, structural changes occur in the liver, which is associated with toxic damage to hepatocytes. Depending on the severity of damage to hepatocytes and liver parenchyma, an increase in the level of enzyme activity (AST, alkaline phosphatase, lactate dehydrogenase, etc.) is detected in the blood. Determining the activity of liver enzymes, the level of bilirubin and its fractions is of particular importance when detecting jaundice, which can be hepatocellular or obstructive in nature.

In acute cholecystitis, significant changes occur in the rheological state of the blood and the hemostasis system: an increase in blood viscosity, the aggregation ability of erythrocytes and platelets, and the coagulation activity of blood. These disorders can lead to disorders of microcirculation and metabolism in the liver and kidneys, creating preconditions for the development of acute liver failure and the occurrence of thromboembolic complications.

B.C. Savelyev, M.I. Filimonov

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